Abstract
The Insulin-like growth factor-I/Insulin-like growth factor-I receptor (IGF-1/IGF-1R) system is a major determinant in colorectal cancer (CRC) pathogenesis. Probiotics (Bifidobacterium longum, BF) and lycopene (LYC) have been individually researched for their beneficial effects in the prevention of CRC. However, the effect of a combined treatment of microencapsulated BF and LYC on IGF-1/IGF-1R/IGFBPs (Insulin-like growth factor-binding proteins) expression in an azoxymethane (AOM)-dextran sulfate sodium (DSS)-induced CRC model have not been demonstrated. BF was microencapsulated by the spray drying technique, with high viability, and daily gavaged with LYC for 16 weeks to CD-1 mice in an AOM-DSS model. The results indicated that BF- and BF + LYC-treated groups had significantly lower inflammation grade, tumor incidence (13–38%) and adenocarcinoma (13–14%) incidence compared to the AOM + DSS group (80%), whereas LYC treatment only protected against inflammation grade and incidence. Caecal, colonic and fecal pH and β-glucuronidase (β-GA) values were significantly normalized by BF and LYC. Similarly, BF and BF + LYC treatments significantly reduced both the positive rate and expression grade of IGF-1 and IGF-1R proteins and normalized Insulin-like growth factor-binding protein-3 (IGFBP3) expression. Based on intestinal parameters related to the specific colon carcinogenesis in an AOM-DSS-induced model, LYC and microencapsulated BF supplementation resulted in a significant chemopreventive potential through the modulation of IGF-1/IGF-1R system.
Highlights
Cancer is a genetic disorder characterized by an altered balance between proliferation and mechanisms of cell death
The results indicated an improvement by Bifidobacterium longum (BF) and LYC treatments, as well as by metformin administration, in intestinal parameters related to specific colon carcinogenesis in the AOM-dextran sulfate sodium (DSS) model
Lycopene (LYC) is a carotenoid that selectively stimulates the growth of probiotics in the gastrointestinal tract (GIT) and potentiates the beneficial effects of these microorganisms [5]
Summary
Cancer is a genetic disorder characterized by an altered balance between proliferation and mechanisms of cell death. The evidence highlights the insulin/IGF system as an important molecular target for the pathogenesis, progression and treatment of CRC. IGF-1 factor is found to be more highly expressed in adenocarcinomas compared to adenomas and normal colon samples from patients, while IGFBP3 is lower in patients than in healthy individuals [2,3]. This strongly suggests a positive and a negative association of these two proteins with CRC risk, respectively. The levels of these IGF system components might play a central role in cell-cycle progression, differentiation, and proliferation in CRC. The underlying pathophysiological links are still barely understood, and the molecular mechanisms still remain unsolved
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